Acute bacterial prostatitis

From AAUS
Jump to: navigation, search

Author

U-Syn Ha (Department of Urology, Seoul ST. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea)

Executive Summary

Epidemiology and pathogenesis

1. Prostatitis syndromes are a very common presentation in the clinical setting and tend to occur in young and middle-aged men.

Diagnosis

1. Patients with acute bacterial prostatitis present with typical signs and symptoms of an acute urinary tract infection including irritative and/or obstructive voiding complaints, and have additional symptoms of systemic infections like malaise, nausea, vomiting, chills and fever, and sometimes present with signs of symptoms of urosepsis. They also complain of perineal and suprapubic pain due to a painful swollen prostate and may have associated pain or discomfort of the external genitalia (GR: B).

2. Digital rectal examination reveals a hot, boggy, and exquisitely tender prostate gland (GR: B).

3. Prostatic massage for the expression of prostatic fluid is not indicated and perhaps even harmful because it could precipitate bacteremia or sepsis (GR: B).

4. A midstream urine specimen is sufficient and will show prominent leukocyturia and bacteriuria with typical uropathogens (GR: B).

5. The sonographic determination of residual volume is an important diagnostic procedure, because infravesical obstruction may play an important pathogenic role in acute bacterial prostatitis (GR: B).

6. Transrectal ultrasound (TRUS) does not need to be performed on every patient with suspected acute bacterial prostatitis (GoR B), but can aid in the diagnosis or exclusion of a prostatic abscess (GR: B).

7. Computer tomography (CT) and magnetic resonance imaging (MRI) offer no advantage over TRUS, unless the abscess has penetrated the confines of the prostate gland or there are further abscess foci suspected (GR: B).

8. PSA is moderately to markedly elevated in a patient with acute bacterial prostatitis, but is not a diagnostic requirement (GR: C).

9. In patients with elevated PSA serial measurement is recommended as a useful tool for follow-up (GR: B).

10. Escherichia coli is the most common pathogen encountered in acute prostatitis (GR: B).

11. There is a significantly higher rate of mixed infection in prostatitis from prior manipulation as compared with spontaneous acute prostatitis (GR: B).

Treatment

1. Rapid initiation of broad-spectrum parenteral antibiotics and symptomatic support are mandatory for the patients with acute bacterial prostatitis (GR: B).

2. Supportive measures include i.v. hydration and catheter drainage if the patient cannot void (GR: B).

3. Insertion of a suprapubic cystotomy tube is the optimal therapy for relief from urinary obstruction (GR: B).

4. In-and-out catheterization to relieve the initial obstruction or short-term (< 12 hours) indwelling catheterization with a small-caliber Foley catheter is appropriate (GR: B).

5. The selection and course of antibiotics should be adjusted according to the pathogens isolated and the results of bacterial susceptibility testing (GR: B).

Prostate abscess

1. Suspicion of a developing abscess is raised if there is no response to appropriate antibiotic therapy, and can be confirmed by TRUS (GR: B).

2. If prostatic abscess is discovered, initiation of broad-spectrum antibiotics and prompt surgical drainage is crucial (GR: B).

Introduction

Acute bacterial prostatitis constitutes a urologic emergency. It is uncommon and usually occurs in concert with a UTI but can have a dramatic presentation. Usually, many clinicians diagnose and treat the acute bacterial prostatitis empirically. A correct diagnosis has therapeutic implications since acute prostatitis may require a longer course of treatment than other forms of urinary tract infection and because the choice of antibiotic to complete treatment after fever subsides should be based on its ability to penetrate into prostatic tissue. Thus, it is of great necessity to define detailed and consensual diagnosis and treatment criteria for acute bacterial prostatitis.

Methodology

We surveyed the extensive literature regarding acute bacterial prostatitis available in Medline via Pubmed and also considered other relevant publications up to July 2014. We used terms prostatitis, bacterial prostatitis, acute bacterial prostatitis, combined with the terms: diagnosis, evaluation, management or treatment, for the search strategy. For the purpose of this review a total of 72 possibly eligible publications were included into the analysis, which were screened by title and abstracts. The limitations for this literature search were English language (two eligible publications were not fully reviewed because just only abstracts were written in English). The papers were rated according to the level of evidence and the strength of recommendations according to ICUD standards. [1][2].

Definition of the disease

Overview

Acute bacterial prostatitis represents an acute infection of the prostate gland. It is a male urinary tract infection (UTI) that has some features in common with lower UTI in females, including the etiological organisms involved and some of their urovirulence factors. The host response, however, is very different from simple cystitis and the treatment course is more complicated[3]. The prostatitis syndrome is a common healthcare issue affecting 10–14% of men of all ages and ethnicities. Acute bacterial prostatitis is associated with severe, mainly Gram-negative infection[4]. In the 1999, NIH consensus statement on prostatitis, prostatitis and prostatitis-like symptoms were classified into four broad categories[5]. Type I prostatitis refers to acute bacterial prostatitis.

Epidemiology

Overall, prostatitis syndromes are a very common presentation in the clinical setting and tend to occur in young and middle-aged men. However, acute bacterial prostatitis accounts for the rarest category among the NIH classification. It is diagnosed in less than 0.02% of all patients seen for prostatitis[6]. However, the potential morbidity and mortality of acute prostatitis constitutes a true urologic emergency[7]. It is characterized by an acute onset of pain combined with irritative and obstructive voiding symptoms in a patient with manifestations of a systemic febrile illness. The hospital admission rate for acute bacterial prostatitis in the USA in 1994 was 12.7 in 100,000 as the first, second or third principal diagnosis for hospital admission[8](LE: 4).

Characterization

Etiology

Acute bacterial prostatitis is the result of severe infection of mainly Gram-negative bacteria, which can be easily isolated from the urine. Escherichia coli is the most common pathogen encountered in acute prostatitis, accounting for 87% of cases[9][10][11][12][13]. However, other pathogens include Pseudomonas, Proteus, Klebsiella, Streptococcus, Enterobacter, and Staphylococcus. Mixed flora infections can occur in 2.5% of cases[9]. Some investigators reported causative microorganisms as below. Escherichia coli (64%), Enterococcus (7%), Pseudomonas (6%) and other Gram-negative rods (12%)[11][14](LE: 3). The spectrum of microbial etiologies reported is similar to those found in complicated female UTI, both in the case of community-acquired infections (two third of Enterobacteriacae sp, 5–10% of Enterococcus sp and P. aeruginosa) as well as for nosocomial infections (large proportion of resistant bacteria) [15][16](LE: 3). The prevalence of venereal agents are low, reported as 2%. These results do not support the recommendations suggesting to treat first for Neisseria gonorrhoeae and Chlamydia trachomatis in young adults[17][18][19].

Risk factors

The mechanisms of Acute bacterial prostatitis are reflux of infected urine into the ejaculatory and prostatic ducts, an ascending urethral infection from the distal urethra, meatus and bladder direct or lymphatic invasion from the rectum, and hematogenous infection[20][21] Although many patients with acute bacterial prostatitis have no clear risk factors, underlying functional or anatomical anomalies that predispose to urogenital infections might affect the development of prostatitis. Prior manipulation of the lower urinary tract including chronic indwelling bladder catheterization, intermittent bladder catheterization, urodynamic study, transurethral surgery and prostate biopsy could be predisposing factors[22][23][24][25].

Clinical Evaluation/risk assessment

Diagnostic and staging procedures

The diagnosis of acute bacterial prostatitis does not generally present much difficulty for the urologist[26](LE: 4) and it is usually based on typical signs and symptoms[27]. Patients with symptoms of acute bacterial prostatitis have to undergo urinalysis and culture of the urine. An initial imaging of the prostate is suggested to exclude prostatic abscess [28](LE: 4).

Symptoms and signs

There are no common key symptoms of acute bacterial prostatitis. The NIH revised classification of prostatitis deals more with pathophysiology and laboratory diagnosis and describes the clinical features of acute bacterial prostatitis only briefly as "signs of acute UTI"[5](LE: 4). Irritative and/or obstructive voiding complaints including dysuria, urinary frequency and urgency are typical[5](LE: 4). Obstructive voiding complaints including hesitancy, poor interrupted stream, and even acute urinary retention are common. The patients complain of perineal and suprapubic pain and may have associated pain or discomfort of the external genitalia. The patients have a swollen prostate that is extremely painful when investigated. Patients with acute bacterial prostatitis are often acutely ill and distressed. Symptoms of systemic infection like malaise, nausea, vomiting, chills and fever may vary. These patients may even be systemically toxic, i.e. flushed, febrile, tachycardic, tachypnoic, hypotensive, and present even with all signs and symptoms of an urosepsis[5][6][21][29](LE: 4). Digital rectal examination reveals a hot, boggy, exquisitely tender and tense prostate gland. Fluctuation during palpation is suspicious for prostatic abscess. Defecation may cause pain[27]. Perineal pain and anal sphincter spasm may complicate the digital rectal examination[29][30](LE: 4). Although a gentle rectal examination can be performed in patients who have suspected acute bacterial prostatitis, prostatic massage for the expression of prostatic fluid is not indicated and perhaps even harmful because it is painful for the patient and it could precipitate bacteremia or sepsis[4][21][29][30](LE: 4).

Urine analysis and culture

In patients presenting with acute bacterial prostatitis, a midstream urine specimen will show prominent leukocyturia and bacteriuria[27]. Midstream urine culture is considered the only laboratory evaluation of the lower urinary tract and usually shows typical uropathogens [28][31](LE: 4).

The NIH revised classification of prostatitis does not include the "four-glass-test" for diagnosis[5], because prostatic massage is not recommended during the early phase of acute bacterial prostatitis (see above)[32][33]. Moreover, expressed prostatic secretion (EPS) or voided bladder 3 urine (VB3) are not necessary because the diagnosis can be made from symptomatic presentation and midstream urine culture[7](LE: 4, GR: C).

Functional findings

The sonographic determination of residual volume is an essential diagnostic procedure, because infravesical obstruction may play an important pathogenic role in acute bacterial prostatitis[34][35](LE: 3). And the difference in voiding problems may reflect age differences and the prostate volume. In addition, the frequency of voiding problems, particularly urinary retention, was remarkably higher in the group that underwent prior manipulation[25](LE: 3). Some investigators suggested that bladder outlet obstruction might not be the main cause of acute bacterial prostatitis[36](LE: 3). For this reason, more evidence is necessary to clarify the relationship between obstructive bladder dysfunction and acute bacterial prostatitis.

Imaging studies

No routine clinical, biological or imaging test can currently provide evidence that adequately rules out prostatic involvement in male UTI[17]. The French guideline and one American guideline just consider that "any UTI in male has the potential for a prostatic involvement"[37][38][39][40][41][42](LE: 4).

There are only a few studies that describe ultrasonographic findings in non-abscessed acute prostatitis[43][44][45][46]. Recently, in a prospective study of 45 patients with a clinical diagnosis of acute bacterial prostatitis, transrectal ultrasound (TRUS) was performed upon admission as well as one month after antibiotic therapy and the findings correlated with the clinical presentation of disease [40]. The authors conclude that TRUS does not need to be performed on every patient with suspected acute bacterial prostatitis (as only 47% had sonographically demonstrable lesions on admission and 61% had lesions improved or disappeared post treatment), but TRUS would be indicated to exclude the presence of prostatic abscess (LE: 2a, GR: B). In conclusion, carefully performed TRUS can aid in the diagnosis or exclusion of a prostatic abscess without increasing the risk for urosepsis[40](LE: 2a, GR: B).

Current reports indicate that the more cost-intensive computer tomography (CT) and magnetic resonance imaging (MRI) offer no advantage over TRUS, unless the abscess has penetrated the confines of the prostate gland or there are further abscess foci suspected[34][35] (LE: 3).

In some papers, the investigators stated that intraprostatic color flow in patients with acute prostatitis was greater than in the normal prostate, or those with chronic inflammation or carcinoma[47](LE: 3). According to the study, in most of the patients, the vascularity of the prostate was increased in the acute phase of inflammation (15-spot scale). With recovery from infection color flow in the prostate decreased to  15 spots, the pattern in healthy men[48](LE: 3). Hypoechoic areas in the peripheral zone of the prostate can persist for a long time in patients with acute prostatitis. Color doppler ultrasonography of these areas can helps to differentiate them from those with carcinoma[49].

There are also two interesting imaging studies – one performed with prostatic Indium-labeled leukocyte scintigraphy and one performed with a combination of PSA levels and TRUS-provided evidence supporting a frequent involvement of the prostate in male UTI[50][51](LE: 2a).

The former was carried out to determine whether indium-111 (111In)-labelled leukocytes (ILLs) accumulated in the infected tissue and whether uptake responded to treatment[52]. Scintigraphs prior to antibiotic treatment showed uptake in prostates of all patients with acute bacterial prostatitis; after treatment no uptake was noted in nine out of 10 patients, and one out of 10 had markedly decreased uptake. In the patients with UTI, if there was no involvement in the prostate, no uptake occurred in prostates. ILLs could be useful for detecting acute bacterial prostatitis in the future[28].

The latter showed the prostate is concurrently involved in men with febrile UTI with a transient increase in prostate volume and serum PSA during the acute stage of disease[43][51](LE: 3). With these two concepts, the presence of an inflammatory reaction within the prostate can inform us of acute prostatitis when the diagnosis is not clear[17].

Serum prostate-specific antigen (PSA)

Although prostate-specific antigen (PSA) levels are not a mainstay of diagnosis, they are generally moderately to markedly elevated in the setting of acute bacterial prostatitis[53][54][55](LE: 3). The role of serum PSA in the differential diagnosis and evaluation of acute bacterial prostatitis is not clear. But elevated levels of PSA have been described in 70% of men with acute bacterial prostatitis[56](LE: 3) as a consequence of increased vascular permeability and disrupted epithelium of the gland. In a prospective study of 39 men with pyrexia (>38.3 °C), serum PSA levels were used to categorize patients according to an initial diagnosis of acute bacterial prostatitis, pyelonephritis, urogenital infection or fever of unknown origin. All of the 20 cases with pyrexia and elevated PSA were diagnosed and treated as acute bacterial prostatitis[53]. Game´ et al.[57]demonstrated a decreased free-to-total (f/t) PSA ratio up to 30 days following adequate antimicrobial therapy, indicating the significance of increased bound PSA in acute prostatitis[57](LE: 3). The decrease of f/t PSA ratio has been correlated to systemic inflammation as measured by serum C reactive protein (CRP) levels. In a prospective study of 70 men with febrile UTI with prostatic involvement as measured by tPSA, this marker has been proven useful to assess prostatic infection. Effective treatment with antibiotics resulted in significantly reduced serum PSA. A decline of tPSA levels in patients after appropriate antimicrobial treatment has been suggested to indicate a healing process[43](LE: 3). So the authors recommend PSA as a concise, accurate, rapid and cost-effective tool for identifying acute bacterial prostatitis and for follow-up[28](GR: B).

Treatment

Patients with acute bacterial prostatitis are easily diagnosed and successfully treated with appropriate antibiotic therapy and possible urinary drainage, as long as the clinician keeps a high index of suspicion for prostatic abscess in patients who fail to respond quickly[29][30](LE: 4).

Principles of management

Use of antibiotics

Appropriate management of acute bacterial prostatitis includes rapid initiation of broad-spectrum parenteral antibiotics and symptomatic support [49]. Treatment of acute bacterial prostatitis is well standardized. Current guidelines for the treatment of acute bacterial prostatitis have only been worked out by the EAU[37][42](LE: 4).

Pharmacologic penetration of antibiotics in the acutely inflamed prostatic tissue is considered to be sufficient in the case of susceptible bacteria. In severe cases, parenteral administration of high doses of bactericidal antibiotics, such as a broad-spectrum penicillin derivative, a third-generation cephalosporin with or without aminoglycosides, or a fluoroquinolone, is required until fever and other parameters of acute infection are normalized. It can be performed alone or in combination with supportive measures including i.v. hydration and catheter drainage if the patient cannot void[25][58](LE: 4).

In less severe cases, an oral fluoroquinolone for 10 days may be sufficient[34](LE: 4). The selection and course of antibiotics can be adjusted according to the pathogens isolated and the results of bacterial susceptibility testing[26].

In most cases the fever resolves in 36–48 h[49][49](LE: 2a-4). After successful initial therapy, switching to an oral regimen such as a fluoroquinolone is appropriate. The oral antibiotic therapy should be continued at least for a total of two to four weeks[37][42](LE: 4) although currently there is no consensus on the optimal treatment duration.

The duration of therapy for acute prostatitis has not been well studied. If the patient is responding clinically and the pathogen is sensitive to treatment, most experts recommend that antibiotic therapy be continued for three to four weeks to prevent relapse, although a longer course is sometimes necessary[59](LE: 4, GR: C). A patient with acute bacterial prostatitis must be over-treated rather than under-treated [60](LE: 4, GR: C). Kravchick et al. reported that three months after the end of a six-week therapy, EPS cultures were still positive in a third of the men. Prolonged therapy (at least six weeks) and subsequent follow-up with Stamey’s test at the three-monthly visits are required to prevent early recurrence[49](GR: B).

Antibiotic resistance

In a recent guideline for antibiotic treatment of acute bacterial prostatitis, the administration of cephalosporins or a quinolone alone or in combination with an aminoglycoside has been recommended[37][42](LE: 4).

The susceptibility to ciprofloxacin of E. coli was shown to be relatively low (76.2%) in some local areas[25](LE: 3). A result as such probably reflects the increase in resistant bacteria owing to the recent excessive use of ciprofloxacin at that local area. The guidelines for the treatment of urinary tract infection of the Infectious Disease Society of America (IDSA) published in 1999 do not recommend a specific antibiotic for empirical treatment when the local level of resistance among E. coli strains exceeds 20%. The IDSA also emphasizes that physicians should obtain information about local resistance rates[25][61](GR: C).

As in the previous report, ciprofloxacin alone may be an inadequate choice, especially in patients with prior manipulation of the urinary tract. Considering the very low susceptibility to cephalosporins (< 60%) in pathogens other than E. coli, and the relative high isolation rates (> 40%) of pathogens other than E. coli, cephalosporins as single therapeutic agents may have limited use in this community. Most commonly, antibiotic combination therapy for acute bacterial prostatitis includes a cephalosporin and an aminoglycoside. The second- and third-generation cephalosporins have been prescribed relatively frequently for this purpose. Administration of an aminoglycoside must be confined to the group of patients without prior manipulation owing to their susceptibility. In the group of patients with prior manipulation in which pathogens other than E. coli constitute a substantial number of isolates, a combination of a cephalosporin and amikacin should be recommended for empirical therapy[25](GR: B).


Additional points to be considered

Another supportive treatment options like alpha-blockers, antipyretics or anti-inflammatory agents may be beneficial, although current data are lacking.3 Stool softeners are also recommended[21](GR: C).

Some investigators reported that empirical antibiotic treatments lead to inadequate antibiotic treatment in 42% of the cases and a higher rate of bacteriological failure. Moreover, the clinical failure rate being much higher than the bacteriological failure rate suggests that antibiotic treatment frequently induces an incomplete resolution of the symptoms, even without any early infection relapse, possibly because of a persistent underlying urological disorder[17](GR: B).

In the previous study of acute prostatitis, the abnormalities requiring surgical correction were detected in 24% of the patients after a check-up including digital rectal examination, prostatic ultrasound, post-void residual urine measurement and uroflow measurement[51](GR: B).

Follow-up and monitoring

Although the role of serum prostate-specific antigen (PSA) in the differential diagnostic evaluation of acute bacterial prostatitis is not finally proven, elevated PSA is common. Effective treatment with antibiotics results in significantly reduced serum PSA. Therefore some authors recommend PSA as a concise, accurate, rapid and cost-effective tool for identifying acute bacterial prostatitis and for the follow-up[28][31] (LE: 4).

After antibiotic treatment, the long-term response is unclear. A prospective study found a bacterial persistence rate at three months of 33% [49] (LE: 2a). Therefore, prolonged therapy of fluoroquinolones for six weeks and reevaluation after that has been recommended[49](GR: B). In this manner, patients with acute prostatitis tend to have persistent infection. Acute prostatitis tends to persist and bacterial localization cultures should be taken at subsequent follow-up visits for at least three months[49]. Along with this, PSA levels could be high even up to three months after an acute episode[49](GR: B).

Morote et al.[62]showed that acute inflammation contributed to PSA increases but did not influence the percentage of free PSA in patients with cancer-free biopsies (LE: 3). Moreover, some patients with carcinoma could be missed during the acute phase of inflammation. Therefore, PSA and TRUS monitoring are strongly recommended (GR: B).

Special considerations

Prostate abscess

Prostatic abscesses are uncommon but potentially serious manifestations of acute infection of the prostate and demand prompt treatment. It represents a severe complication of acute bacterial prostatits with an estimated incidence of 2–18%[36](LE: 3) and a mortality rate of 3–30%. Antibiotic treatment of acute bacterial prostatitis is simple but abscess formation is well described and may have devastating sequelae. Its clinical diagnosis is somewhat difficult and suspicion of a developing abscess is raised if there is no response to appropriate antibiotic therapy, and can be confirmed by TRUS[59](LE: 4). TRUS should not be postponed for > 48 h in patients who do not respond to appropriate antibiotic therapy[49](GoR B). This is particularly important for the patients with immunocompromised disease or diabetes[28][40](GR: C). Patients who are immunocompromised, especially patients who have HIV/AIDS, seem to be more susceptible to the development of acute bacterial prostatitis and to the occurrence of a potentially life-threatening prostatic abscess. The incidence rate rises to roughly 14% in those who have developed AIDS[63](LE: 3). If a prostatic abscess is discovered, initiation of broad-spectrum antibiotics and prompt surgical drainage is crucial[7][64](GR: C).

Microbiology of prostatic abscess

E. coli and Staphylococcus species are the most commonly isolated pathogens in prostatic abscess, although other pathogens, such as Mycobacterium tuberculosis, Actinomyces, Citrobacter, Bacteroides fragilis, Aeromonas aerophyla, and Klebsiella pneumonia have been reported[35][65][66][67][68][69](LE: 3). Burkholderia pseudomallei overwhelmingly predominates in the Thai population[68].

How to treat the prostatic abscess

Recommended treatment of prostatic abscess consists of broadspectrum antibiotic coverage and, in most cases, drainage of the abscess. Several surgical procedures have been described to relieve abscess formation. Transurethral incision or resection, suprapubic adenectomy, perineal incision and transrectal or transperineal prostatic puncture and drainage under sonographic guidance have been applied according to location and extension of the abscess[34][35](GR: C & B).

Transperineal incision and drainage[70]must be considered when the abscess has penetrated beyond the prostatic capsule or penetrated through the levator ani muscle[29][30](GR: C). Although transurethral unroofing and perineal drainage were once the mainstays of surgical drainage, transrectal ultrasound-guided aspiration of prostatic abscesses has been increasingly used as an effective means of drainage that may avoid the potential morbidity associated with transurethral drainage[65][71](GR: B). Some authors also support urinary diversion with a suprapubic catheter[35][66].

In small abscesses, patients may be treated conservatively by the administration of antibiotic agents together with the placement of a suprapubic catheter. The follow-up requires regular TRUS controls[34][35](GR: C & B).

Relief from obstruction

In acute bacterial prostatitis, urinary obstruction is a very common symptom. Because patients can have significant obstruction from an acutely inflamed prostate, bladder scanning for postvoid residual urine is recommended. If the residual urine is less than 100 mL, the patient should be initiated on alpha blocker therapy; if the residual is large, consideration should be given to placement of a small urethral catheter if short-term drainage is required or a suprapubic catheter if longer-term drainage is required[6][7](GR: B).

Traditionally, it has been suggested that the insertion of a suprapubic cystotomy tube is the optimal therapy because an indwelling Foley catheter may further obstruct urethral ducts, resulting in the potential to develop prostate abscesses[62][63][64](LE: 4). In most patients, however, an in-and-out catheterization to relieve the initial obstruction or short-term (<12 hours) indwelling catheterization with a small-caliber Foley catheter is appropriate[30](GR: C).

Abbreviation

URI: urinary tract infection, EPS: expressed prostatic secretion, VB3: voided bladder 3 urine, TRUS: transrectal ultrasound, CRP: C reactive protein, PSA: prostate-specific antigen

References

  1. Abrams, P., S. Khoury, and A. Grant, Evidence--based medicine overview of the main steps for developing and grading guideline recommendations. Prog Urol, 2007. 17(3): p. 681-4.
  2. U.S. Department of Health and Human Services Public Health Service Agency for Health Care Policy and Research, 1992: p. 115-127.
  3. !!! INVALID CITATION !!!
  4. 4.0 4.1 Naber, K.G., Management of bacterial prostatitis: what's new? BJU Int, 2008. 101 Suppl 3: p. 7-10.
  5. 5.0 5.1 5.2 5.3 5.4 Krieger, J.N., L. Nyberg, Jr., and J.C. Nickel, NIH consensus definition and classification of prostatitis. Jama, 1999. 282(3): p. 236-7.
  6. 6.0 6.1 6.2 Wagenlehner, F.M., et al., The role of antibiotics in chronic bacterial prostatitis. Int J Antimicrob Agents, 2005. 26(1): p. 1-7.
  7. 7.0 7.1 7.2 7.3 Benway, B.M. and T.D. Moon, Bacterial prostatitis. Urol Clin North Am, 2008. 35(1): p. 23-32; v.
  8. US Department of Health and Human Services Public Health Service, National Center for Health Statistics. National Hospital Discharge Survey Public Use Data Tape Documentation 1994. 1996, Hyattsville, MD: Centers for Disease Control and Prevention.
  9. 9.0 9.1 Collins, M.M., et al., How common is prostatitis? A national survey of physician visits. J Urol, 1998. 159(4): p. 1224-8.
  10. Stamey, T.A., Pathogenesis and treatment of urinary tract infections. 1980, Baltimore ; London: Williams & Wilkins. ix,612p.
  11. 11.0 11.1 L'opez-Plaza, L. and Bostwick DG, Prostatitis. Pathology of the prostate, ed. D.G. Bostwick. 1990, New York: Churchill Livingstone.
  12. Dowling, K.J., J.A. Roberts, and M.B. Kaack, P-fimbriated Escherichia coli urinary tract infection: a clinical correlation. South Med J, 1987. 80(12): p. 1533-6.
  13. Stamey, T.A., Pathogenesis and treatment of urinary tract infections. 1980, Baltimore: Williams & Wilkins.
  14. L'opez-Plaza, L. and D.G. Bostwick, Prostatitis, in Pathology of the prostate, D.G. Bostwick, Editor. 1990, Churchill Livingstone: New York.
  15. Zhanel, G.G., et al., Antibiotic resistance in outpatient urinary isolates: final results from the North American Urinary Tract Infection Collaborative Alliance (NAUTICA). Int J Antimicrob Agents, 2005. 26(5): p. 380-8.
  16. Caron, F., [Bacteriologic diagnosis and antibiotic therapy of urinary tract infections]. Rev Prat, 2003. 53(16): p. 1760-9.
  17. 17.0 17.1 17.2 17.3 Etienne, M., et al., Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infect Dis, 2008. 8: p. 12.
  18. Krieger, J.N., S.O. Ross, and J.M. Simonsen, Urinary tract infections in healthy university men. J Urol, 1993. 149(5): p. 1046-8.
  19. Domingue, G.J., Sr. and W.J. Hellstrom, Prostatitis. Clin Microbiol Rev, 1998. 11(4): p. 604-13.
  20. Kirby, R.S., et al., Intra-prostatic urinary reflux: an aetiological factor in abacterial prostatitis. Br J Urol, 1982. 54(6): p. 729-31. 21. Meares, E.M., Jr., Prostatitis. Med Clin North Am, 1991. 75(2): p. 405-24.
  21. 21.0 21.1 21.2 21.3 Roberts, R.O., et al., A review of clinical and pathological prostatitis syndromes. Urology, 1997. 49(6): p. 809-21.
  22. Wyndaele, J.J., Complications of intermittent catheterization: their prevention and treatment. Spinal Cord, 2002. 40(10): p. 536-41.
  23. Mosharafa, A.A., et al., Rising incidence of acute prostatitis following prostate biopsy: fluoroquinolone resistance and exposure is a significant risk factor. Urology, 2011. 78(3): p. 511-4.
  24. Ozden, E., et al., Incidence of acute prostatitis caused by extended-spectrum beta-lactamase-producing Escherichia coli after transrectal prostate biopsy. Urology, 2009. 74(1): p. 119-23.
  25. 25.0 25.1 25.2 25.3 25.4 25.5 Ha, U.S., et al., Acute bacterial prostatitis in Korea: clinical outcome, including symptoms, management, microbiology and course of disease. Int J Antimicrob Agents, 2008. 31 Suppl 1: p. S96-101.
  26. 26.0 26.1 Wagenlehner, F.M. and K.G. Naber, [Therapy of prostatitis syndrome]. Urologe A, 2001. 40(1): p. 24-8.
  27. 27.0 27.1 27.2 Neal, D.E., Acute bacterial prostatitis, in Textbook of prostatitis, J.C. Nickel, Editor. 1999, Isis Medical Media: Oxford. p. 115-122.
  28. 28.0 28.1 28.2 28.3 28.4 28.5 Weidner, W. and R.U. Anderson, Evaluation of acute and chronic bacterial prostatitis and diagnostic management of chronic prostatitis/chronic pelvic pain syndrome with special reference to infection/inflammation. Int J Antimicrob Agents, 2008. 31 Suppl 1: p. S91-5.
  29. 31.0 31.1 Weidner, W., et al., Acute bacterial prostatitis and chronic prostatitis/chronic pelvic pain syndrome: andrological implications. Andrologia, 2008. 40(2): p. 105-12.
  30. Lau, C.S. and Sant GR, Urethritis, Prostatitis, Epididymitis, and Orchitis, in Infectious diseases, S.L. Gorbach, J.G. Bartlett, and N.R. Blacklow, Editors. 2004, Lippincott Williams & Wilkins: Philadelphia ; London. p. xxix, 2515 p., [2] p. of plates.
  31. Lau, C.S. and G.R. Sant, Urethritis, prostatitis, epididymitis, and orchitis, in Infectious diseases, S.L. Gorbach, J.G. Bartlett, and N.R. Blacklow, Editors. 2004, Lippincott Williams & Wilkins: Philadelphia.
  32. 34.0 34.1 34.2 34.3 34.4 Ludwig, M., Diagnosis and therapy of acute prostatitis, epididymitis and orchitis. Andrologia, 2008. 40(2): p. 76-80.
  33. 35.0 35.1 35.2 35.3 35.4 35.5 Ludwig, M., et al., Diagnosis and therapeutic management of 18 patients with prostatic abscess. Urology, 1999. 53(2): p. 340-5.
  34. 36.0 36.1 Millan-Rodriguez, F., et al., Acute bacterial prostatitis: two different sub-categories according to a previous manipulation of the lower urinary tract. World J Urol, 2006. 24(1): p. 45-50.
  35. 37.0 37.1 37.2 37.3 Naber, K.G., Bishop MC, and Bjerklund-Johansen TE, The management of urinary and male genital tract infections, in European Association of Urology Guidelines, E.G. Office, Editor. 2006, Drukkerij Gelderland: Arnhem, The Netherlands. p. 1-126.
  36. Société de Pathologie Infectieuse de Langue Française (SPILF), Deuxième conférence de consensus en thérapeutique anti-infectieuses: antibiothérapie des infections urinaires. Médecine et Maladies infectieuses, 1991: p. 51-4.
  37. Rubin, R.H., et al., Evaluation of new anti-infective drugs for the treatment of urinary tract infection. Infectious Diseases Society of America and the Food and Drug Administration. Clin Infect Dis, 1992. 15 Suppl 1: p. S216-27.
  38. 40.0 40.1 40.2 40.3 Horcajada, J.P., et al., Transrectal prostatic ultrasonography in acute bacterial prostatitis: findings and clinical implications. Scand J Infect Dis, 2003. 35(2): p. 114-20.
  39. Société de Pathologie Infectieuse de Langue Française, Deuxieme conference de consensus en therapeutique anti-infectieuse antibiotherapie des infections urinaires 16 Novembre 1990. Médecine et Maladies Infectieuses, 1991. 21(2, Part 2): p. 51-54.
  40. 42.0 42.1 42.2 42.3 Naber, K., et al., The management of urinary and male genital tract infections. European Association of Urology. European Association of Urology Guidelines. Arnhem: Drukkerij Gelderland, 2006: p. 1-126.
  41. 43.0 43.1 43.2 Ulleryd, P., et al., Prostatic involvement in men with febrile urinary tract infection as measured by serum prostate-specific antigen and transrectal ultrasonography. BJU Int, 1999. 84(4): p. 470-4.
  42. Resnick, M.I., Ultrasonic evaluation of the prostate and bladder. Semin Ultrasound, 1980(1): p. 69.
  43. Millan Rodriguez, F., et al., [Management of acute prostatitis: experience with 84 patients]. Arch Esp Urol, 1995. 48(2): p. 129-36.
  44. Rifkin, M.D. and Resnick ML, Ultrasonography of the prostate, in Ultrasonography of the urinary tract, M.I. Resnick and M.D. Rifkin, Editors. 1991, Williams & Wilkins: Baltimore, Md. p. xviii, 502 p.
  45. Veneziano, S., P. Pavlica, and D. Mannini, Color Doppler ultrasonographic scanning in prostatitis: clinical correlation. Eur Urol, 1995. 28(1): p. 6-9.
  46. Cho, I.R., et al., Prostate blood flow characteristics in the chronic prostatitis/pelvic pain syndrome. J Urol, 2000. 163(4): p. 1130-3.
  47. 49.0 49.1 49.2 49.3 49.4 49.5 49.6 49.7 49.8 49.9 Kravchick, S., et al., Acute prostatitis in middle-aged men: a prospective study. BJU Int, 2004. 93(1): p. 93-6.
  48. Velasco, M., et al., Accurate topographical diagnosis of urinary tract infection in male patients with (111)indium-labelled leukocyte scintigraphy. Eur J Intern Med, 2004. 15(3): p. 157-161.
  49. 51.0 51.1 51.2 Ulleryd, P., et al., Selective urological evaluation in men with febrile urinary tract infection. BJU Int, 2001. 88(1): p. 15-20.
  50. Mateos, J.J., et al., 111Indium labelled leukocyte scintigraphy in the detection of acute prostatitis. Nucl Med Commun, 2002. 23(11): p. 1137-42.
  51. 53.0 53.1 Hara, N., et al., Application of serum PSA to identify acute bacterial prostatitis in patients with fever of unknown origin or symptoms of acute pyelonephritis. Prostate, 2004. 60(4): p. 282-8.
  52. Schaeffer, A.J., et al., Treatment of chronic bacterial prostatitis with levofloxacin and ciprofloxacin lowers serum prostate specific antigen. J Urol, 2005. 174(1): p. 161-4.
  53. Neal, D.E., Jr., et al., Prostate specific antigen and prostatitis. I. Effect of prostatitis on serum PSA in the human and nonhuman primate. Prostate, 1992. 20(2): p. 105-11.
  54. Pansadoro, V., et al., Prostate-specific antigen and prostatitis in men under fifty. Eur Urol, 1996. 30(1): p. 24-7.
  55. 57.0 57.1 Game, X., et al., Total and free serum prostate specific antigen levels during the first month of acute prostatitis. Eur Urol, 2003. 43(6): p. 702-5.
  56. Schaeffer, A.J., Diagnosis and treatment of prostatic infections. Urology, 1990. 36(5 Suppl): p. 13-7.
  57. 59.0 59.1 Nickel, J.C., Prostatitis: evolving management strategies. Urol Clin North Am, 1999. 26(4): p. 737-51.
  58. Stevermer, J.J. and S.K. Easley, Treatment of prostatitis. Am Fam Physician, 2000. 61(10): p. 3015-22, 3025-6.
  59. Warren, J.W., et al., Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women. Infectious Diseases Society of America (IDSA). Clin Infect Dis, 1999. 29(4): p. 745-58.
  60. 62.0 62.1 Morote, J., et al., Effect of inflammation and benign prostatic enlargement on total and percent free serum prostatic specific antigen. Eur Urol, 2000. 37(5): p. 537-40.
  61. 63.0 63.1 Leport, C., et al., Bacterial prostatitis in patients infected with the human immunodeficiency virus. J Urol, 1989. 141(2): p. 334-6.
  62. 64.0 64.1 Santillo, V.M. and F.C. Lowe, The management of chronic prostatitis in men with HIV. Curr Urol Rep, 2006. 7(4): p. 313-9.
  63. 65.0 65.1 Chou, Y.H., et al., Prostatic abscess: transrectal color Doppler ultrasonic diagnosis and minimally invasive therapeutic management. Ultrasound Med Biol, 2004. 30(6): p. 719-24.
  64. 66.0 66.1 Varkarakis, J., et al., Three-dimensional ultrasound guidance for percutaneous drainage of prostatic abscesses. Urology, 2004. 63(6): p. 1017-20; discussion 1020.
  65. Oliveira, P., et al., Diagnosis and treatment of prostatic abscess. Int Braz J Urol, 2003. 29(1): p. 30-4.
  66. 68.0 68.1 Aphinives, C., et al., Prostatic abscesses: radiographic findings and treatment. J Med Assoc Thai, 2004. 87(7): p. 810-5.
  67. Tai, H.C., Emphysematous prostatic abscess: a case report and review of literature. J Infect, 2007. 54(1): p. e51-4.
  68. Granados, E.A., et al., Prostatic abscess: diagnosis and treatment. J Urol, 1992. 148(1): p. 80-2.
  69. Gogus, C., et al., The value of transrectal ultrasound guided needle aspiration in treatment of prostatic abscess. Eur J Radiol, 2004. 52(1): p. 94-8.